Monthly Archives: August 2011 - Page 3

The PHD Food Plate

We thought we’d skip our usual food post today and instead ask for your opinion on the first draft of our Perfect Health Diet Food Plate.

But first, a few links. At the Ancestral Health Symposium Shou-Ching and I were delighted to meet Josephine and Henry Svendblad, who run the excellent Nutty Kitchen. We’ve been fans of Josephine and Henry since we first discovered their blog a year ago, and the respect is mutual. They told us that they’ve been tagging some of their recipes with a “Perfect Health Diet” tag. (Also their “Paleo 2.0” tagged dishes are PHD-compliant. Actually, everything at their site is PHD-compliant as far as I can tell.) It’s a great source for recipe ideas.

Also, our regular commenter Gary has created a site with easy, quick Perfect Health Diet recipes at his site, 10 Minute Meal. He explained in a recent comment:

I get enthusiastic about PHD and tell my friends about it, but the most frequent response I’d get was that it may be great, but it means home cooking everything. I’d counter that home cooking isn’t hard. So finally I set up a small website that shows how I’ve done my own interpretation of a PHD meal plan and the home cooking that make it possible to do it during the week, working 50-hour weeks and making 2 or 3 meals a day for me and my spouse.

If ten minute meals are what you’re looking for, check out Gary’s site.

Our Food Plate

The US government introduced its food plate earlier this year:

It seems a little simple, even for the US government.

We wanted to see if we could do better. Here’s our first draft (click to enlarge):

We’re very interested in your reaction. Does it give an accurate idea of the diet? How would you improve it?

Around the Web; Post-AHS Edition

It’s been a good few weeks for the Paleo movement, but it’s nice to get back to normal. Around the Web is back!

[1] Upcoming Chris Kresser podcast: Chris Kresser and Danny Roddy will be recording a podcast with me on Friday morning. Chris is soliciting questions and requests for topics of discussion at The Healthy Skeptic.

[2] Interesting posts: You can find round-ups of AHS reminiscences at Richard Nikoley and Diana Hsieh’s Paleo Rodeo.

Stephan has an outstanding “critical examination” of “the carbohydrate hypothesis of obesity”. Briefly, Gary Taubes is correct that obesity is characterized by defects in body fat regulation (Part I), but leptin rather than insulin pathways are most important, and insofar as insulin matters it is insulin resistance that is the culprit because insulin promotes weight loss (Part II), and the most effective diets for causing obesity are not those with the highest carb consumption (>65%), but those with intermediate carb consumption (~50%) (Part III).

Chris Highcock of Conditioning Research found some fascinating papers this week:

  • In dogs, obesity leads to a lowering of body temperature. This is neither new nor surprising but paired with Stephan’s point that insulin increases thermogenesis and resting energy expenditure, it highlights that factors other than insulin are critical to obesity.
  • Dieting makes you fat: The more times obese people lost 5 kg or more, the more they later weighed. I think this is more evidence that malnourishment promotes obesity. Calorie restriction is fine, but only if nutrients are not restricted.
  • Bacterial infections are less likely to lead to memory loss in rats that exercise. Perhaps exercise protects the integrity of the blood-brain barrier, keeping bacteria out of the brain.

Seth Roberts reports that cleaning products such as Febreze can cause migraines and cranky mood. Vinegar and baking soda is a safer way to clean.

Travis Culp at PaleoHacks looks at connections between fructose and leptin.

The New York Times reports that microdoses of chocolate – about one-sixth of an ounce / 5 gm daily – can increase exercise performance and fitness, and that antibiotic-resistant infections are becoming much more common in children. Antibiotic-resistant skin infections generally begin as a red pimple that is often wrongly assumed to be a spider bite.

Every once in a while someone writes to ask me if they should fear a high-fat diet because of CarbSane’s writings on lipotoxicity. I reply that lipotoxicity only appears after metabolic syndrome has developed and, while it may drive the transition from obesity to diabetes, it is not a cause of obesity, and not a danger to people who don’t have metabolic syndrome. Also, the implications for diet are not obvious, since carb intake suppresses NEFA clearance from the blood and enhances glucotoxicity. The literature commonly speaks of “glucolipotoxicity” to describe this compounded toxicity problem. CarbSane hasn’t always been clear on these points, so it’s good to see an excellent post from her covering the basics.

Via Marginal Revolution, MIT researchers have found a possible universal treatment for viral infections: an engineered drug that enters cells and, when it encounters the double-stranded RNA of reproducing viruses, causes the cell to commit suicide. Dead cells can then be replaced by uninfected new cells via the body’s normal wound repair process. My first thought is this sounds great for curing viral diseases, but I wonder if it would shorten lifespan.

Melissa McEwen links omega-6 fats to acid reflux.

Michael Smith of Critical MAS offers a variation on the Leangains approach to fitness.

Barry Sears argues that a weight loss diet should be rich in salmon.

[3] In the hunt: John Durant’s talk on zoos at AHS – and the difficulty of creating natural environments for the animals – made me think of this photo we took on our visit to the San Diego Zoo Safari Park. Here is a cheetah chasing its favorite plush toy:

[4] Cute animal photo:

Via Yves Smith.

[5] Disturbing thought:

George Orwell suggested that the fancier the restaurant, the more people have dripped sweat into your food.

Via Huffington Post.

[6] Shou-Ching’s photo art:

[7] A strong man:

Via Conditioning Research.

[8] When good cholesterol goes bad: Via Jan Petersen, an excellent talk on lipoproteins:

[9] Video of the week: Grizzly vs bichon:

Gary Taubes and Stephan Guyenet: Three Views on Obesity

In a post titled “Ancestral Health Symposium Drama”, Stephan Guyenet begins to expound his scientific differences with Gary Taubes.

Since my views differ a bit from both Stephan and Gary, I thought readers might enjoy a third view.

My General Perspective on Obesity

My view is that obesity is caused in the first place by malnutrition, toxins, and infections. Each can contribute in multiple ways:

  • Malnutrition can affect appetite and energy utilization. Micronutrient deficiencies will increase appetite, regardless of energy balance. Macronutrient deficiencies may also do this. The resulting increased calorie intake may be only partially balanced by increased activity and thermogenesis; fat gain in caloric surplus tends to be more weakly opposed by brain regulatory circuits than muscle loss during caloric deficit. Malnutrition can impair energy utilization by several pathways: for instance, loss of mitochondrial antioxidants may lead to oxidative damage that impairs mitochondrial health. Choline deficiency induces metabolic syndrome and obesity (see Choline Deficiency and Plant Oil Induced Diabetes, Nov 12, 2010). Long-term, malnutrition may induce methylation defects which affect epigenetic regulation of metabolism. These can be passed on from mother to child.
  • Toxins also have multiple pathways by which they induce obesity. For example, diets that combine fructose or alcohol with polyunsaturated fats are very effective at producing metabolic syndrome and obesity in animals, and food opioids affect the endocannibinoid pathways which can be important in obesity and appetite regulation. See Why We Get Fat: Food Toxins (Jan 20, 2011) and Wheat and Obesity: More from the China Study (Sep 4, 2010) for more.
  • Infections have also been linked to obesity. I’ve blogged about how adenovirus infections of adipose cells promote obesity (Obesity: Often An Infectious Disease, Sep 22, 2010), but another very important pathway is from gut infections to obesity. Briefly, gut pathogens release fat-soluble toxins which can enter systemic circulation, and also modulate immune function. Toxins from pathogens have been shown to induce metabolic syndrome in the liver, promoting obesity. Via the immune system, gut flora can promote obesity. I’ve briefly mentioned one pathway (in Thoughts on Obesity Inspired by Stephan, Jun 2, 2011): gut immune modulation in the gut has been shown to determine whether adipose tissue macrophages are in a pro-inflammatory or anti-inflammatory state. A pro-inflammatory state promotes obesity. Research into the many ways gut flora influence obesity is in early stages, but it’s clearly important.

Due to the diversity of factors which conspire to cause obesity, it is a rather heterogeneous disease. Its unifying character is that some combination of causal factors induces “metabolic damage,” such as leptin resistance, in a variety of organs, including the brain. Metabolic damage can affect both appetite regulation and energy homeostasis.

I’ve discussed Stephan’s views and food reward theory (Thoughts on Obesity Inspired by Stephan, Jun 2, 2011). Food reward theory offers a plausible explanation for many aspects of obesity. I agree that food reward is an important factor in obesity, but consider it one among several factors, and believe that different factors may dominate in different people. Also, it seems likely to me that food reward becomes a dominant factor in obesity only after some form of metabolic damage from malnutrition, toxins, or infections begins to affect the brain’s regulatory systems. In a healthy person a highly palatable diet might have little effect on weight for quite some time. Nor am I convinced that low food reward diets are necessarily the best approach for long term weight loss or for the health of the obese, though I do believe they are great for short-term weight loss.

Distinguishing my view from Stephan’s is difficult because the obesity-inducing diets used in animal studies are generally both toxic and malnourishing and highly palatable. The “cafeteria diet” of Cheetos and such – rich in wheat, sugar, and vegetable oil – is an example.

I haven’t previously blogged about Gary’s views, but I consider very low carb dieting to be an imperfect solution for good health generally. (NB: Low-carb, which I endorse, is for me 400-600 carb calories, very low-carb, which I deprecate, is <200 calories.) Ketogenic diets may be beneficial in some cases of obesity, but I believe they should still include some starchy carbohydrates.

The Exchange

Stephan has transcribed the Q&A between Gary and himself and offers revised answers. I’ll insert my thoughts:

GT: How does your food reward hypothesis hypothesis explain a culture in which mothers are obese and their children are starving?  Are the mothers eating Snickers bars and not sharing them with their children?

SG: The food reward/palatability hypothesis of obesity is not mine, it’s a hypothesis that originated in the 1970s, perhaps earlier, and is a major subject of ongoing obesity research.  I don’t expect it to explain every instance of obesity.  Obesity involves multiple factors, an important one of which is food reward and palatability.  That being said, you have to examine a culture’s food habits in some detail, both before and after a change in obesity prevalence, to determine if reward/palatability may have played a role.  I don’t know enough about that specific culture to judge whether food reward would have played a role there.

PJ: Famines occur in impoverished societies with disrupted social institutions. People in these cultures are driven to eat the cheapest calories, which are the toxic grains such as wheat. They also tend to be malnourished, especially during famines. Malnutrition and toxic foods can create the disease of obesity, especially in a suitable infectious disease context.  Once the disease of obesity is induced, periods of caloric availability lead to weight gain which may be defended during subsequent famines. This explains maternal obesity persisting during a period of food scarcity. The slenderness of their children is a result of the disease process not having had enough time to work. It may take decades for malnutrition and food toxicity to induce obesity in the child.

So the element of long-acting causal factors and history eliminates the apparent conflict between an obese mother and a starving slender child.

Because food reward could induce obesity in the mother prior to the famine which is defended later, and food reward may act differently in growing children, food reward theory may be able to explain the situation. But Stephan prudently allows for the possibility that other causes of obesity besides food reward may be at work.

GT: The Pima indians were obese in 1902, following 20-30 years of famine.  How would your theory explain this?

SG: The Pima were first contacted in 1539 by the Spanish, who apparently found them to be lean and healthy.  At the time, they were eating a high-carbohydrate, low-fat diet based on corn, beans, starchy squash, and a modest amount of gathered animal and plant foods from the forest and rivers in the area.  In 1869, the Gila river went dry for the first time, and 1886 was the last year water flowed onto their land, due to upstream river diversion by settlers.  They suffered famine, and were rescued by government rations consisting of white flour, sugar, lard, canned meats, salt and other canned and processed goods.  They subsequently became obese.  Their diet consisted mostly of bread cooked in lard, sweetened beverages and canned goods, and they also suddenly had salt.  I don’t see why that’s incompatible with the food reward hypothesis.  It is, however, difficult to reconcile with the carbohydrate hypothesis.

PJ: The Pima Indian story seems compatible with both Stephan’s and my views, since they ate a nourishing, low-toxicity, low-food reward diet when they were lean but a malnourishing, toxic, high-food reward diet when they became obese. It seems incompatible with Gary’s ideas, since the Pima ate a high-carb diet at all times. Thus it’s a bit surprising Gary is so fond of the Pima story. It weakens, not helps, his case.

GT: There are two possible hypotheses here.  The alternative hypothesis is that sugar and refined carbohydrate consumption changes the regulation of fat tissue, leading to obesity.  The studies you cited in which people lost weight by consuming bland liquid diets would have been low in sugar as well.  “We need an observation that can refute one of the two hypotheses”.

SG: The bland liquid diet in Hashim et al. that caused massive weight loss is called “Nutrament”.  It is 50% carbohydrate, 30% fat and 20% protein.  The primary three sources of carbohydrate in this formulation are lactose (from milk), sucrose (table sugar) and corn syrup.  The bland liquid used in the study by Cabanac et al. (Renutryl), which also caused weight loss, was high in refined glucose and sucrose.  I find this rather difficult to reconcile with the idea that sugar and refined carbohydrate are inherently obesogenic.

PJ:  It’s unclear to me what Gary’s “alternative hypothesis” is. Why are refined carbohydrates different from unrefined carbohydrates? Both may raise blood glucose and insulin levels similarly. If toxic plant foods are the problem, then he should say toxins rather than carbohydrates are the problem. If it’s the macronutrient that’s the problem, why does refining matter?

Stephan scores a point against both Gary and me here, but especially against Gary, since the liquid diets are fairly high in carbs. As there was some sucrose and polyunsaturated fat, this was not a non-toxic diet, and I don’t know if adequately micronutrients were provided – probably not – but on its face the food reward theory seems to work best in explaining this experiment.

GT: “How was it bland then?”

SG: The diet was a liquid formulation that (judging by the ingredients) probably tastes like powdered milk.  The subjects were drinking that for 100% of their calories.  That fits any reasonable definition of a low reward/palatability diet, regardless of the sugar.

GT: What about the Mexican-Americans in Star county, Texas, who were obese despite the fact that there was only one restaurant in the whole town?

SG: Again, you have to examine a culture’s food habits in some detail, both before and after a change in obesity prevalence, to determine if reward/palatability may have played a role.  I don’t know enough about that specific culture to judge whether food reward would have played a role there.

GT: How can we differentiate between altered palatability and altered carbohydrate intake as important factors in the rising obesity prevalence of industrializing nations?

SG: Increased carbohydrate intake is a particularly poor explanation for obesity in industrializing populations, as the majority of them (for example, most of Asia and Africa) are going from a diet very high in carbohydrate, to one that is lower in carbohydrate and higher in fat.  There are also a smaller number of cultures that developed obesity as they went from high-fat to higher carbohydrate, industrialized food.  Therefore, the ideas that carbohydrate or fat are inherently fattening don’t appear consistent with the evidence as a whole.  An alternative explanation whereby both fat and carbohydrate, as well as other factors, are important for reward/palatability, an excess of which contributes to obesity, fits the evidence better.

PJ: It seems to be easiest to induce obesity with a roughly equal mix of carbs and fat; both low-carb and low-fat diets tend to be less obesogenic. This result is compatible with Stephan’s views because carb and fat together are more rewarding than either alone, and with my views because carb-fat combinations can be highly toxic – for instance, a fructose-PUFA combination is more toxic than either alone; or carbs feed gut pathogens while fats carry their toxins into the body.

It is unclear how Gary would explain the evidence from both animal studies and human populations that obesity becomes more likely as high-carb diets shift toward more fat.

Of Glass Houses

Stephan is a model of scholarly virtue, so Gary’s challenge at the end of his talk was a shock. I thought Stephan’s original reply – “Thank you for the advice” – was perfect, but Stephan revises it:

GT: “I would just recommend in the future you should pay attention to populations that might refute your hypothesis rather than just presenting populations that support.  That’s always key in science.”

SG: People who live in glass houses shouldn’t throw stones.

Presumably Stephan is challenging Gary to address some of the populations who seem to refute his hypothesis: Asian populations that have become more obese while dropping carbs from 75% to 50% of diet, or the Pima who remained lean on a high-carb diet for centuries.

In other words, to seek a theory that can explain all phenomena, as a scientist should.

In general, I find Gary’s work rhetorically artful but not very helpful to scientific progress. He often neglects to consider the full implications of his own evidence. This is especially true when he ventures into molecular and cellular biology.

For instance, he uses genetic lipodystrophies to illustrate that fat storage can be a disease of molecular biology, rather than excess food consumption. Now, the mutations in these lipodystrophies are generally not in insulin, the insulin receptor, or even centrally located on insulin pathways. So the lipodystrophies show that other molecules besides insulin can be responsible for fat storage (or negative regulation of fat storage), and may be relevant to obesity.

But when he looks into which molecules might be responsible for obesity, he offers only one candidate: insulin.

More startling is his neglect of perhaps the single most important molecule in obesity, leptin. Stephan writes:

[H]e sent me a manuscript for his book Why We Get Fat and asked for my advice prior to its publication.  I explained to him that he needed to use the word “leptin” in the book, particularly when discussing animal models of obesity that are obese because of defects in leptin signaling (ob/ob mice and Zucker rats, for example).

This is just like his use of lipodystrophies: mice get obese due to mutations in leptin, but he doesn’t discuss the role of leptin, preferring to keep the spotlight on insulin.

I don’t want to sound harsh because I think Gary is on the side of the angels. He has done very beneficial work refuting saturated-fat-phobia and encouraging low-carb diets, which improve the health of nearly all westerners who adopt them (although the reason is probably reduced toxicity from wheat and sugar, rather than reduced carbohydrate calories).

But I think he would do well to be more generous to others. I was excited when he began blogging, but disappointed by his first post:

conventional wisdom … almost incomprehensibly naïve and wrong-headed … nonsensical notion … I’ve been consistently amazed at the ability of researchers … to accept some of the rote ideas … without seemingly giving it any conscious thought whatsoever, or without wanting to ask the kinds of questions that a reasonably smart junior high school student should ask if given the opportunity…. I don’t understand this failure of intellect … nonsensical explanations … he falls short, as he’s working outside his area of expertise … we’re being fed nonsense … we will typically pass that nonsense along … If the experts had ever been open to a little skeptical thinking from others or had they been appropriately skeptical themselves … What’s been needed (and still is) was for someone (a reasonably smart 14-year-old would suffice) to ask the obvious questions and then insist on intelligent answers.

I find such talk ungenerous; and ironic, because in places in that very post Gary’s own reasoning is unsound.

Biology is complex, none of us have all the answers, and a lifetime is too short to acquire all the answers. Since we have no choice but to live in glass houses, we should all be humble, and refrain from casting stones.

The Ancestral Health Symposium

We’re back from the California and the Ancestral Health Symposium, which was a fantastic meeting – the most enjoyable symposium I’ve attended. Brent Pottenger, Aaron Blaisdell, and the host of volunteers who assisted them deserve tremendous credit for organizing it. Bravo!

It had the feel of a Paleo Woodstock: the leading names in the movement were gathered in one place for the first time, and there was a festive atmosphere, especially on the first day and at a pre-event party hosted by Aaron Blaisdell. For Shou-Ching and I, it was a delight to meet in person friends we had come to know through the Internet. We were pleased to meet some of our commenters – and had lunch with one, Mia.

Those who didn’t attend will be able to catch up on it later: presentation slides may be found here; videos of the talks and interviews will be posted here.

People and Pictures

Already there’s a great deal of information about the meeting online. Some participants were active twitterers – check out the Twitter tag #AHS11 for a blow-by-blow account of the meeting. I’m sure many attendees will be posting their own appreciations in coming days, but here are links to some of the early birds:

Richard Nikoley took a lot of pictures at Aaron’s Thursday night party and has more photos in his appreciation of the symposium. PaleoHacks has a thread for pictures from the meeting and a thread for recommendations about talks. Emily Deans has posts about talks and people.

Melissa McEwen, Stephan Guyenet, Chris Masterjohn, Jamie Scott, Andreas Eenfeldt, and Matt Metzgar have posts.

Many at the meeting remarked on how good looking the attendees were. You can find appreciations of looks from Melissa (“the conference was full of beautiful people”), Jamie (“I have never been around so many beautiful people in one room as I have been this past weekend.”), and Stephan (“I was very impressed by the appearance of the attendees”).

I was equally impressed, but that observation leads me to one more. Nearly everyone at the meeting had at one time been following bad diets and had to seek out Paleo. In Denise Minger’s talk, she asked how many people had been vegetarians at one time, and a startlingly large number raised their hands. To discover a healthy way of living, in a world full of mistaken information and unhealthy foods, is possible only for inquisitive, intelligent, discerning people. This was not only a beautiful, but a smart, crowd.

And so very friendly and cheerful. Good health, I believe, leads to good spirits. It was a pleasure to be around everyone, both during the meeting and after hours.

The Talks

A brief summary of the the most notable talks I saw:

S. Boyd Eaton kicked off the conference as the only speaker without a competitor in the parallel track; a well-deserved honor in light of his pioneering role in the Paleo movement. He spent only ten minutes on diet and moved on to expressing a quixotic hope for decreases in the global population in order to restore a more Paleo-like environment. Among the highlights was a picture from the Korean DMZ, a 400-square mile depopulated area that has apparently regained a flourishing wildlife.

Loren Cordain followed with an excellent talk, most of which will be familiar to his fans. I liked his talk a lot, in part because his slides on hunter-gatherer food intakes support our macronutrient ratios.

Staffan Lindeberg gave an excellent talk that also revisited material from his work. A few factoids: blame for the invention of vegetable oils goes to David Wesson, who figured out how to detoxify cotton seeds in 1899, thus giving us “Wesson oil”; and autopsy studies show that at age 40 most people already have atherosclerosis, a disease that is non-existent in wild animals and thus is presumably caused by industrial diets.

Robb Wolf finished the morning session and was his usual dynamic self. Shou-Ching, who hadn’t yet listened to one of his podcasts, was impressed.

If Friday morning felt like a celebrity fest, Friday afternoon was the meat of the symposium. Two Friday afternoon talks were among the best of the meeting.

Emily Deans’s talk was magnificent, pulling together a rich thread of material. Jamie Scott gave an inside look at the practical side of improving health in a corporate setting.

Dr. BG and Dr Tim Gerstner gave an outstanding talk, one of the best of the meeting. Dr BG’s story was fascinating and fast-paced. She and her sister are writing a book, “Jillian’s story,” about Dr BG’s autistic niece who has seen great improvements from chelation therapy. Heavy metal toxicity is an important subject and it looks like Dr BG and her collaborators are going to make an important contribution. We went to dinner Friday night with Dr BG, her sister, Dr Gerstmar, and J. Stanton of gnolls.org, and had a wonderful time.

In attending these two great talks, I missed two of the star attractions of the meeting – Stephan Guyenet, whose talk I would dearly love to have seen, and Gary Taubes. The buzz of the main ballroom when we got back was that Gary had, in the question session, cut to the front of the question line in order to challenge Stephan in some fashion. I expect this video will be the most downloaded one of the conference. UPDATE: Video of Gary’s questioning is here and a detailed account here.

Curious to hear about Stephan’s talk, we had returned to the main ballroom during the break, and stayed to watch Michael Eades. He gave a very nice talk focusing on the pre-history of the Paleo diet – going back to some early clinicians, one of whom was a friend of Vilhjalmur Stefansson, who had tried low-carb Paleo diets on their patients with success.

Again, I was torn between two great speakers as I very much wish I could have heard the talk of anthropologist Craig Stanford, who was opposite Eades. I had a pleasant chat with Dr. Stanford at Aaron’s pre-meeting party and it turns out our professional paths seem to be criss-crossing: I am working on a book on evolutionary biology, applying my economics ideas to the problem, and he is considering writing a book on diet. Small world!

Friday’s last talk was by Chris Masterjohn, who gave a superb exposition on LDL receptors, how LDL-R status can influence LDL time in the blood and oxidation status and, therefore, health. I had read most of the material on Chris’s blog, but still took copious notes. Chris is a most impressive and well-organized speaker.

On Saturday I started with Seth Roberts and Tucker Max. Seth’s talk was excellent – the gist can be found in recent blog posts, such as the one on butter reducing his coronary calcium score.

Tucker Max’s talk was fascinating in light of Todd Hargrove’s recent guest post here (How to Do Joint Mobility Drills, July 26, 2011). Tucker’s idea was that violence, both against animals (hunting) and people (warfare, homicide), must have been a critical factor shaping Paleolithic culture, and that this had important implications: Paleolithic peoples must have spent a lot of time play fighting as practice and as a fitness technique; and they must have developed philosophies, like those associated with all modern martial arts, to develop calmness and serenity in the face of violence – since the natural human reaction, panic, is unhelpful. It sounds as though mobility and serenity practices such as Tai Chi or yoga, which Todd endorsed, and components of religions such as Zen Buddhism may be modern descendants of Paleolithic martial arts. I liked this talk because it reminds us that “ancestral health” encompasses more than diet.

Mat Lalonde’s talk was outstanding. The subject of food toxins is extremely important for health, under-researched by scientists, and lacking in good overviews. (Step Two of our book is among the best, but only scratches the surface.) Mat reviewed research on a number of major food toxins, and discussed the ability of these toxins to survive cooking, enter the body, and contribute to disease. The talk had only one disappointment: Mat dis-associated himself from what he called “your movement.”

Mark Sisson and Denise Minger gave two of the most pleasant, fun talks at the meeting, as befits their super-positive personalities. Luckily on Saturday the two sessions were in neighboring rooms and it was possible to see some of each.

Nora Gedgaudas gave an excellent talk on the use of diet as a clinical approach to mental health disorders. It had plenty of citations that I’m eager to track down. We are fans of ketogenic dieting for neurological diseases, and Nora obviously is too – indeed she promotes a diet that verges on zero-carb. I think this will work well as a fast-acting therapy until she meets a patient with toxoplasmosis or some similar protozoal brain infection, but that the benefits of ketosis have to be balanced against long-term risks of glucose deficiency.

Melissa McEwen gave a fantastic talk about the evolution of the gut. It was fact-filled, science-rich, and entertaining. Interesting part: there is significant human variability in, for instance, colon size and structure. This is important because the digestive tract is really the only part of the body that evolves in response to changing diets. There has been some talk about different populations needing different diets; Melissa’s work suggests that instead of “metabolic typing” we may some day do “gut typing” to determine an optimal personal diet.

John Durant gave an entertaining and informative talk on the history and future of zoos. We had just visited San Diego Zoo and the San Diego Zoo Safari Park (formerly Wild Animal Park) earlier that week, and the Bronx, Washington DC, and Cleveland zoos fairly recently, so I enjoyed John’s take.

Andreas Eenfeldt and Richard Nikoley were another duo that were hard to choose between. Richard is entertaining at all times, and Andreas had an interesting story about the low-carb diet revolution in Sweden. I tried to catch both talks as best as I could.

After fitness talks from Doug McGuff, Frank Forencich, and Erwan LeCorre we chatted with friends new and old before leaving for the airport for our redeye flight back home. Shou-Ching pulled out her camera for a few photos. Here’s one:

All in all, a fabulous meeting. I think the Ancestral Health Society is going to have a big impact, and can’t wait for AHS 2012. Thanks, Aaron, Brent, and everyone else responsible for this enjoyable event!